Like Rick I must disavow any claim to expertise with the DXM approach in attempting to delay/arrest neurodegeneration. All I can claim is some familiarity with the literature and my own subjective experience, along with brief conversations with Dr. Hong in 2006 at the World Parkinson's Congress and by phone. When I told him that I was taking DXM in cough syrup using the single low dose at bedtime protocol recommended by the low-dose naltrexone people, his main concern seemed to be that the preparation contain only DXM as the active ingredient, and to particularly avoid any which contain polystyril which is added to slow down the release of the DXM into the circulation. He seemed to be subscribing to the idea put forth by Zagon that the drug should only briefly bind cell surface receptors proir to the natural early morning time of optimal release of endogenous opioids by the cells.

The pharmacokinetics of DXM (rates of its tissue transport, metabolism and excretion) would certainly have substantial effects on body levels of the drug following its administration. About all I know about these processes is that DXM is very rapidly absorbed, that it readily crosses the blood-brain barrier, and that one of its main metabolites is a hydroxy derivative which Hong has previously shown to be equal to the parent drug in supressing microglial activation.

As Rick has already mentioned, DXM interacts with MDMA receptors, which are known to have effects on the release of dopamine and other neurotransmitters. His suggestion that the apparent on-extending effects that he and Laura have experienced are related to these receptors certainly seems plausible to me.

I presently restrict my use of DXM to the bedtime routine. Although I currently do not experience well-defined "offs", I would be open to experimenting with additional daytime dosing if they were to develop, especially if you, Rick and Laura, continue to see definite benefit in it.

Robert